دورية أكاديمية

New insights in the pathogenesis of immunoglobulin A vasculitis (Henoch-Schönlein purpura).

التفاصيل البيبلوغرافية
العنوان: New insights in the pathogenesis of immunoglobulin A vasculitis (Henoch-Schönlein purpura).
المؤلفون: Heineke MH; Department of Molecular Cell Biology and Immunology, VU University Medical Center, De Boelelaan 1109, 1081 HZ Amsterdam, The Netherlands; Amsterdam Infection & Immunity Institute, Amsterdam, The Netherlands., Ballering AV; Department of Molecular Cell Biology and Immunology, VU University Medical Center, De Boelelaan 1109, 1081 HZ Amsterdam, The Netherlands; Amsterdam Infection & Immunity Institute, Amsterdam, The Netherlands., Jamin A; National French Institute of Health and Medical Research (INSERM) U1149, Centre de Recherche Sur l'Inflammation, 16 Rue Henri Huchard, Paris 75018, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Faculté de Médecine, Site Xavier Bichat, 16 Rue Henri Huchard, Paris 75018, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France., Ben Mkaddem S; National French Institute of Health and Medical Research (INSERM) U1149, Centre de Recherche Sur l'Inflammation, 16 Rue Henri Huchard, Paris 75018, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Faculté de Médecine, Site Xavier Bichat, 16 Rue Henri Huchard, Paris 75018, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France., Monteiro RC; National French Institute of Health and Medical Research (INSERM) U1149, Centre de Recherche Sur l'Inflammation, 16 Rue Henri Huchard, Paris 75018, France; National French Center of Scientific Research (CNRS) ERL8252, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Faculté de Médecine, Site Xavier Bichat, 16 Rue Henri Huchard, Paris 75018, France; Laboratory of Inflamex Excellency, Faculty of Medicine, Xavier Bichat Site, Paris, France., Van Egmond M; Department of Molecular Cell Biology and Immunology, VU University Medical Center, De Boelelaan 1109, 1081 HZ Amsterdam, The Netherlands; Amsterdam Infection & Immunity Institute, Amsterdam, The Netherlands; Department of Surgery, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands. Electronic address: m.vanegmond@vumc.nl.
المصدر: Autoimmunity reviews [Autoimmun Rev] 2017 Dec; Vol. 16 (12), pp. 1246-1253. Date of Electronic Publication: 2017 Oct 14.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 101128967 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-0183 (Electronic) Linking ISSN: 15689972 NLM ISO Abbreviation: Autoimmun Rev Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam ; New York : Elsevier, c2002-
مواضيع طبية MeSH: IgA Vasculitis/*immunology, Animals ; Antibodies/immunology ; Endothelial Cells/immunology ; Glomerulonephritis, IGA/immunology ; Humans ; Immunoglobulin A/immunology ; Receptors, Fc/immunology
مستخلص: Immunoglobulin A vasculitis (IgAV), also referred to as Henoch-Schönlein purpura, is the most common form of childhood vasculitis. The pathogenesis of IgAV is still largely unknown. The disease is characterized by IgA1-immune deposits, complement factors and neutrophil infiltration, which is accompanied with vascular inflammation. Incidence of IgAV is twice as high during fall and winter, suggesting an environmental trigger associated to climate. Symptoms can resolve without intervention, but some patients develop glomerulonephritis with features similar to IgA nephropathy that include hematuria, proteinuria and IgA deposition in the glomerulus. Ultimately, this can lead to end-stage renal disease. In IgA nephropathy immune complexes containing galactose-deficient (Gd-)IgA1 are found and thought to play a role in pathogenesis. Although Gd-IgA1 complexes are also present in patients with IgAV with nephritis, their role in IgAV is disputed. Alternatively, it has been proposed that in IgAV IgA1 antibodies are generated against endothelial cells. We anticipate that such IgA complexes can activate neutrophils via the IgA Fc receptor FcαRI (CD89), thereby inducing neutrophil migration and activation, which ultimately causes tissue damage in IgAV. In this Review, we discuss the putative role of IgA, IgA receptors, neutrophils and other factors such as infections, genetics and the complement system in the pathogenesis of IgA vasculitis.
(Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: CD89; Fc alpha receptor; Henoch-Schönlein purpura; IgA vasculitis; Immunoglobulin A; Neutrophils
المشرفين على المادة: 0 (Antibodies)
0 (IgA receptor)
0 (Immunoglobulin A)
0 (Receptors, Fc)
تواريخ الأحداث: Date Created: 20171018 Date Completed: 20180129 Latest Revision: 20220318
رمز التحديث: 20231215
DOI: 10.1016/j.autrev.2017.10.009
PMID: 29037908
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-0183
DOI:10.1016/j.autrev.2017.10.009